ArticleSchizophrenia research2014
Evaluation of kynurenine pathway metabolism in Toxoplasma gondii-infected mice: implications for schizophrenia.
Article in Schizophrenia research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
46 citing papers in PubMed, 86 citations in OpenAlex.
- Article
- Article
- Latent Cerebral Toxoplasma Gondii Infection Induces the Kynurenine Pathway and Production of Neurotoxic Metabolites.International journal of tryptophan research : IJTR · 2026Article
- Toxoplasma gondii, suicidal behaviour and suicide risk factors in US Veterans enrolled in mental health treatment.Folia parasitologica · 2025Article
- Diseases Caused by and Behaviors Associated withPathogens (Basel, Switzerland) · 2024Review
- Review
- Role of N-acetylkynurenine in mediating the effect of gut microbiota on urinary tract infection: a Mendelian randomization study.Frontiers in microbiology · 2024Article
- Pathological mechanisms of glial cell activation and neurodegenerative and neuropsychiatric disorders caused byFrontiers in microbiology · 2024Review
- Effects of Toxoplasma gondii infection on cognition, symptoms, and response to digital cognitive training in schizophrenia.Schizophrenia (Heidelberg, Germany) · 2022Article
- Toxoplasma infection in male mice alters dopamine-sensitive behaviors and host gene expression patterns associated with neuropsychiatric disease.PLoS neglected tropical diseases · 2022Article
- Sulfadiazine Plus Pyrimethamine Therapy Reversed Multiple Behavioral and Neurocognitive Changes in Long-Term Chronic Toxoplasmosis by Reducing Brain Cyst Load and Inflammation-Related Alterations.Frontiers in immunology · 2022Article
- Epigenetic Manipulation of Psychiatric Behavioral Disorders Induced byFrontiers in cellular and infection microbiology · 2022Review
- Toxoplasmosis: Targeting neurotransmitter systems in psychiatric disorders.Metabolic brain disease · 2022Review
- Comprehensive Overview ofPathogens (Basel, Switzerland) · 2021Review
- Psychological Stresses in Children Trigger Cytokine- and Kynurenine Metabolite-Mediated Abdominal Pain and Proinflammatory Changes.Frontiers in immunology · 2021Article
- Neurological Infection, Kynurenine Pathway, and Parasitic Infection byFrontiers in immunology · 2021Review
- Review
- Dysregulation of kynurenine metabolism is related to proinflammatory cytokines, attention, and prefrontal cortex volume in schizophrenia.Molecular psychiatry · 2020Article
- Neuroimmune Mechanisms and Sex/Gender-Dependent Effects in the Pathophysiology of Mental Disorders.The Journal of pharmacology and experimental therapeutics · 2020Review
- Catastrophic consequences: can the feline parasite Toxoplasma gondii prompt the purrfect neuroinflammatory storm following traumatic brain injury?Journal of neuroinflammation · 2020Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Toxoplasma gondii, an intracellular protozoan parasite, is a major cause of opportunistic infectious disease affecting the brain and has been linked to an increased incidence of schizophrenia. In murine hosts, infection with T. gondii stimulates tryptophan degradation along the kynurenine pathway (KP), which contains several neuroactive metabolites, including 3-hydroxykynurenine (3-HK), quinolinic acid (QUIN) and kynurenic acid (KYNA). As these endogenous compounds may provide a mechanistic connection between T. gondii and the pathophysiology of schizophrenia, we measured KP metabolites in both the brain and periphery of T. gondii-treated C57BL/6 mice 8 and 28 days post-infection. Infected mice showed early decreases in the levels of tryptophan in the brain and serum, but not in the liver. These reductions were associated with elevated levels of kynurenine, KYNA, 3-HK and QUIN in the brain. In quantitative terms, the most significant increases in these KP metabolites were observed in the brain at 28 days post-infection. Notably, the anti-parasitic drugs pyrimethamine and sulfadiazine, a standard treatment of toxoplasmosis, significantly reduced 3-HK and KYNA levels in the brain of infected mice when applied between 28 and 56 days post-infection. In summary, T. gondii infection, probably by activating microglia and astrocytes, enhances the production of KP metabolites in the brain. However, during the first two months after infection, the KP changes in these mice do not reliably duplicate abnormalities seen in the brain of individuals with schizophrenia.
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Registered trials
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